Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 42 myeloma patients our results confirm the association of light chain proteinuria and renal damage, but suggest that while the amount of light chain excreted is an important factor, only some light chains are nephrotoxic. The excretion of the proximal tubular cell lysosomal enzyme N acetyl B D glucosaminidase was a sensitive index of tubular injury, while the presence of low molecular weight proteinuria (Retinol Binding Protein and Lysozyme) was shown to indicate tubular dysfunction in a kidney sufficiently damaged to produce an impaired GFR. Isolated defects of distal tubular function (acid load response and concentrating ability) were rare. Such changes were seen mainly as part of global renal impairment and were usually associated with such specific pathophysiological conditions as plasma hyperviscosity or tubular crystal deposition. Hypercalcemia had a specific effect on the concentrating ability independent of any impairment of renal acidification.
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PMID:Tubular function in multiple myeloma. 393 70

A boy presenting with a severe congenital nephrotic syndrome diagnosed by histological analysis at the age of 3 weeks was biopsied again 7 years later. The ultrastructural glomerular basement membrane abnormalities depicted in the first biopsy were no longer present in the second one. The number of completely hyalinized glomeruli was not significantly decreased. The GFR remained normal, but a moderate persistent, non-selective proteinuria (800 mg/24 h) was noted without oedema. The patient however developed a progressive perceptive deficit of hearing.
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PMID:Electron microscopic studies in a long-term follow-up of a case of congenital nephrotic syndrome. 396 93

Generalised sepsis was induced in sheep by caecal perforation. Serial measurement of haemodynamic parameters revealed that the subsequent generalised sepsis induced increased cardiac output and decreased systemic resistance comparable to that known to occur in man. Glomerular filtration rate in these animals fell significantly 48 hours after induction of sepsis and there was evidence of tubular damage in the finding of low molecular weight proteinuria and increased clearance of lysozyme. Pathological examination of the kidney revealed normal glomeruli, no consistent changes in tubular cells on light microscopy, negative immunofluorescence, but structural changes in proximal tubular cells on EM. In this model, non-hypotensive sepsis predictably produces damage to proximal tubular cells accompanied by reduction in GFR.
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PMID:Acute renal failure and tubular damage due to sepsis in an animal model. 399 81

Recent studies of relatively large numbers of gravidas with primary renal disease indicate that pregnancy probably does not affect the underlying disease in the absence of overt renal insufficiency or hypertension. Women with renal disease and near normal function have a moderate risk for encountering a rise in blood pressure and decline in renal function during pregnancy, complications that are usually manageable and reversible after delivery. There is a substantial risk, however, that heavy proteinuria and edema formation may occur toward the latter stages of pregnancy, especially in women with preexisting proteinuria, although this complication also usually reverses after delivery and does not affect the underlying renal disease. The question of the effect of pregnancy on renal disease in women with moderate renal insufficiency at the start of pregnancy is unanswerable on the basis of available data. Published reports indicate that severe hypertension is a major complicating factor during pregnancy in many of these women and, on theoretical grounds, may play an important role in aggravating the renal lesion. To resolve this question, studies are required in which prepregnancy levels of GFR are carefully monitored, a specific diagnosis of the underlying renal disease is established, and elevated blood pressure levels are normalized during pregnancy.
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PMID:Pregnancy does not exacerbate primary glomerular disease. 405 Jul 88

Gentamicin is a nephrotoxic agent known to damage the proximal tubule,--a site of low molecular weight (LMW) protein reabsorption and catabolism. The effect of gentamicin was investigated on three LMW proteins--amylase, light chains, and beta 2 microglobulin--and the effects were correlated on the latter to renal function as determined by creatinine clearance (GFR). The renal excretion of beta 2 microglobulin (beta 2M) was studied in 18 patients receiving gentamicin and eight control patients. Both gentamicin and control patients had similar mean ages and serum beta 2M. Twelve of the 18 gentamicin treated patients had marked increases in beta 2M excretion. The mean daily 2 beta microglobulin excretion for the gentamicin treated group was 10,511 microgram while that of the control group was 102 microgram. Serial determinations in 10 of the gentamicin treated patients revealed an increase in beta 2M excretion within 48 hours of starting therapy. No deterioration of GFR was seen in any patient. In four patients, beta 2M excretion decreased while still receiving gentamicin. The renal handling of amylase was found to be normal in four patients and mildly abnormal in three patients receiving gentamicin who also had increased beta 2M excretion. Urinary light chains were determined in four of these seven patients and found to be normal. It is concluded that gentamicin induces an early and often transient tubular proteinuria. This tubular proteinuria is not associated with clinical nephrotoxicity.
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PMID:The significance of beta-2 microglobulinuria associated with gentamicin therapy. 617 9

Intrinsic membrane properties of the glomerular capillary wall were evaluated in 20 diabetic patients, who had heavy proteinuria and reduced GFR, and in 15 healthy control subjects. The glomerular sieving coefficients were determined for narrow dextran fractions with molecular radii between 20 and 64 A. GFR determinants were directly measured or indirectly estimated. These quantities were then subjected to a theoretical analysis based upon (1) a mathematical model of glomerular ultrafiltration and (2) a pore model of transmembrane solute transport. The results indicated that in patients with diabetic nephropathy and glomerular ultrafiltration coefficient (0.02 vs. 0.16 ml . sec-1 . mm Hg-1 . 1.73m-2), effective pore area-to-pore length (2.6 x 10(6) vs. 20.0 x 10(6) cm), and mean pore radius (56.8 vs. 58.0 A) are all reduced relative to normal control subjects. It is suggested that (1) hypofiltration in advanced diabetic nephropathy results, in part, from reduction of the surface area available for filtration, while (2) proteinuria is a consequence of either loss of electrostatic barrier function, of isolated focal disruptions within the glomerular filtration barrier, or a combination thereof.
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PMID:Glomerular function in advanced human diabetic nephropathy. 618 Feb 14

Alterations in glomerular permeability were studied in Adriamycin-induced proteinuria in rats by measuring fractional clearances (C/GFR) of uncharged labeled dextrans of varying molecular radii (ae) and of anionic, native, and cationic horseradish peroxidases (HRP) in experimental and control animals. Experimental animals were studied between days 14 and 55 after a single intravenous dose of Adriamycin (doxorubicin), 7.5 mg/kg. Mean proteinuria in the experimental animals was 98 mg/24 hr. Glomerular morphology showed few changes except for epithelial cell swelling, vacuolization, and foot process obliteration, and a significant reduction of glomerular colloidal iron staining. Polyethyleneimine staining revealed a similar distribution of anionic sites in the laminae rarae interna and externa in proteinuric rats as compared with controls. Inulin clearances revealed reduction in GFR and RPF of 20 and 15%, respectively. Dextran C/GFR values showed in experimental animals a size defect for molecules with an ae exceeding 40 A, with a four- to fivefold increase over the values found in control animals for dextrans with ae of 58 and 60 A. The peroxidase clearances showed a slight increase in C/GFR of anionic HRP in experimental animals, as could be expected on the basis of the sieving defect, whereas the C/GFR values for native and cationic HRP were virtually unchanged, indicating an intact functional charge barrier in the proteinuric animals.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Glomerular permeability and polyanion in adriamycin nephrosis in the rat. 619 86

Patients with idiopathic recurrent calcium nephrolithiasis (n = 57) and controls (n = 16) were investigated regarding the relationship between renal phosphate handling, other renal tubular functions and calcium metabolism. Incomplete renal tubular acidosis (RTA) was disclosed in 13 patients. RTA patients together with stone formers with normal renal acidification capacity (SF) exhibited low values for serum phosphate and renal threshold phosphate concentration (TmP/GFR) compared with controls. TmP/GFR was lower in RTA patients than in stone formers with normal renal acidification. Hypercalciuria of the absorptive type with normal serum PTH and urinary cAMP concentrations was a common finding in both stone patient groups, whereas no patient displayed unequivocal evidence of parathyroid hyperfunction. Fractional excretion of sodium was raised in both SF and RTA patients compared with controls. There was a positive relationship between the fractional excretion of phosphate and sodium in all subjects as a group. TmP/GFR was negatively correlated to fractional excretion of sodium. Twenty-three percent of RTA patients and 8% of SF displayed tubular proteinuria which often was associated with low TmP/GFR levels and enhanced natriuresis. It is concluded that a defective renal tubular phosphate handling is common in calcium stone formers and often associated with signs of other tubular dysfunctions. The altered phosphate handling seems to be unrelated to hypercalciuria.
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PMID:Phosphate metabolism in renal stone formers. (II): Relation to renal tubular functions and calcium metabolism. 627 2

Antirheumatic drugs may cause a significant, although generally reversible, reduction of GFR, RPF, CNa and hyperkalemia in a wide range of extrarenal and renal disease states (severe liver disease, congestive heart failure, SLE, nephrotic syndrome, etc.); chronic ingestion has been associated with analgesic nephropathy. Recently cases have been reported of reversible acute renal failure with massive proteinuria and interstitial nephritis. The acute effects of a renal PG-inhibiting (ibuprofen) or a renal PG-sparing (sulindac) cyclo-oxygenase inhibitor on renal functional parameters (GFR, RPF, CNa, CK, urine volume) and proteinuria have been studied in 24 patients with clinically and biopsy proven chronic glomerular disease; in all patients ibuprofen significantly reduced GFR, RPF, CNa; these changes were fully reversible within a week of withdrawal of the drugs. A causal relationship exists between inhibited PG-synthesis and reduced renal function in these patients, since sulindac, which failed to reduce urinary PG excretion did not alter significantly the renal function. Moreover proteinuria is not reduced by ibuprofen at doses comparable, as far as concerns inhibition of PG-synthesis, to those of indomethacin.
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PMID:Clinical assessment of the renal toxicity of antirheumatic drugs. 633 23

The authors present a contemporary picture of the pathogenesis and clinical course of diabetic nephropathy in type I diabetics describing the stages of the disease and the possible evidence for reversibility of the kidney damage with tight metabolic control. During the so-called latency period, which is clinically non-detectable, the predominant functional abnormalities (increase in GFR with sub-clinical glomerular proteinuria) can be corrected by strict control although there is no evidence for the regression of the associated anatomical changes such as the enlarged filtration area. As for the described increase in thickness of the glomerular basement membrane, from experimental data and pancreatic transplants in man, delay in its development and to some extent regression of the glomerular lesions can be expected. The problem of how the renal lesions in experimental diabetes mirror the changes in the human kidney is discussed. During the symptomatic period, with intermittent and subsequently constant proteinuria and progressive decline in renal function, which are observed in only about 30% of type I diabetics, the role of arterial hypertension and its effective control is emphasized. Finally, the renal failure period is indicative of irreversible damage to the kidneys. The progression from its early to its late stages is variable between different patients but each individual patient shows a constant rate of deterioration. The evidence for the efficacy of medical treatment in slowing down its progression is very limited at present but much can be done to improve the quality of life by dietary measures, treatment of fluid overload and hypertension. When the end-stage diabetic kidney disease is reached, with serum creatinine above 8 mg/dl, renal transplantation from a living donor offers a good chance for a relatively acceptable quality of life for years. In conclusion, it is stressed that the morbidity of diabetic nephropathy could eventually be reduced through effective control of the metabolic abnormalities of diabetes with the methods presently available.
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PMID:The natural history of diabetic nephropathy in type I diabetes and the role of metabolic control in its prevention, reversibility and clinical course. 634 25


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